The Effects Of Glucose Metabolism And TRB3 And P-AKT Expression In Rats Liver During Chronic Intermittent Hypoxia

Objective:observe the effect of glucose metabolism in rats and the expression of Tribbles protein 3(TRB3) and phosphorylated protein kinase B(P-AKT) in rats liver cells during chronic intermittent hypoxia,and explore the related protein P-AKT and TRB3 change in insulin signaling pathway and the possible mechanism of rats insulin resistance during chronic intermittent hypoxia.Methods :Forty healthy male Sprauge-Dawley(SD) 6 weeks old rats were randomly divided into five group, the normal control group was given normal air, chronic intermittent hypoxia 2 weeks group, 4 weeks group, 6 weeks group, 8 weeks group were exposed to in different time periods of intermittent hypoxia environment,with 8rats in each group.all the rats were killed after the exposure time. we measure fasting food glucose and fasting insulin,calculate insulin resistance index(HOMA-IR)according to the formula.To observe the expression of TRB3 and P-AKT protein and the morphological changes in the hepatic,and gray level quantitative analysis with image systemthe,average gray value was represent protein expression.Finally,the data were statistically analyzed.Results:With the intermittent hypoxia exposure time prolonged,compared with NC group,(1) the levels of fasting blood glucose,insulin and HOMA-IR were significantly increased in chronic intermittent hypoxia group,there are significant differences(P < 0.05),and in CIH8 was most significantly,(2) the expression of TRB3 protein increased significantly(P < 0.05), the expression of P-AKT protein was significantly decreased(P < 0.05), and in CIH8 group was more significant.(3)Pearson correlation analysis showed that HMOA-IR and P-AKT was positivelycorrelataed(r=0.903, P < 0.05),and was negatively correlated with TRB3(r =-0.828,P < 0.05).Conclusions:1.SD rats fasting blood glucose,insulin,and the HMOA-IR was higher during chronic intermittent hypoxia,and the liver cell was damaged and the morphology changed.the liver cell occured abnorm glucose metabolism by insulin resistance,the degree of liver cells damage and insulin resistance was more serious with the chronic intermittent hypoxia time prolonged.It indicates that chonic intermittent hypoxia was involved in insulin resistence in liver.2. chronic intermittent hypoxia can make insulin signaling protein TRB3 increased and the downstream protein of Akt decreased, protein expression abnormalities is correlated with HMOA-IR, It indicates that chronic intermittent hypoxia can activate TRB3 protein and inhibit Akt phosphorylation which is involved in the disturbance of glucose metabolism.